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MeSH Disease

Human Phenotype

Transmission

Seroprevalence
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    The impact of COVID-19 in diabetic kidney disease MESHD kidney disease and chronic HP chronic kidney disease MESHD: A population-based study

    Authors: Juan Alonso Leon-Abarca; Roha Saeed Memon; Bahar Rehan; Maimoona Iftikhar; Antara Chatterjee; Andrés Gonzalez-Guerra; Emilio Camafeita; Mariya Lytvyn; María Isabel Guillén; David Sanz-Rosa; Daniel Martín-Pérez; Cristina Sanchez-Ramos; Ricardo Garcia; Juan Antonio Bernal; Sijia Tao; Tristan R Horton; Elizabeth N Beagle; Ernestine A Mahar; Michelle YH Lee; Joyce Cohen; Sherrie Jean; Jennifer S Wood; Fawn Connor-Stroud; Rachelle L Stammen; Olivia M Delmas; Shelly Wang; Kimberly A Cooney; Michael N Sayegh; Lanfang Wang; Daniela Weiskopf; Peter D Filev; Jesse Waggoner; Anne Piantadosi; Sudhir P Kasturi; Hilmi Al-Shakhshir; Susan P Ribeiro; Rafick P Sekaly; Rebecca D Levit; Jacob D Estes; Thomas H Vanderford; Raymond F Schinazi; Steven E Bosinger; Mirko Paiardini

    doi:10.1101/2020.09.12.20193235 Date: 2020-09-16 Source: medRxiv

    Background: The spectrum of pre-existing renal disease MESHD is known as a risk factor for severe COVID-19 outcomes. However, little is known about the impact of COVID-19 on patients with diabetic nephropathy MESHD nephropathy HP in comparison to patients with chronic kidney disease HP chronic kidney disease MESHD. Methods: We used the Mexican Open Registry of COVID-19 patients 11 to analyze anonymized records of those who had symptoms related to COVID-19 to analyze the rates of SARS-CoV-2 infection MESHD, development of COVID-19 pneumonia HP pneumonia MESHD, admission, intubation, Intensive Care Unit admission and mortality. Robust Poisson regression was used to relate sex and age TRANS to each of the six outcomes and find adjusted prevalences SERO and adjusted prevalence SERO ratios. Also, binomial regression models were performed for those outcomes that had significant results to generate probability plots to perform a fine analysis of the results obtained along age TRANS as a continuous variable. Results: The adjusted prevalence SERO analysis revealed that that there was a a 87.9% excess probability of developing COVID-19 pneumonia HP pneumonia MESHD in patients with diabetic nephropathy MESHD nephropathy HP, a 5% excess probability of being admitted, a 101.7% excess probability of intubation and a 20.8% excess probability of a fatal outcome due to COVID-19 pneumonia HP pneumonia MESHD in comparison to CKD patients (p<0.01). Conclusions: Patients with diabetic nephropathy MESHD nephropathy HP had nearly a twofold rate of COVID-19 pneumonia HP pneumonia MESHD, a higher probability of admission, a twofold probability of intubation and a higher chance of death once admitted compared to patients with chronic kidney disease HP chronic kidney disease MESHD alone. Also, both diseases had higher COVID-19 pneumonia HP pneumonia MESHD rates, intubation rates and case-fatality rates compared to the overall population. Keywords: COVID-19, SARS-CoV-2, Chronic Kidney Disease MESHD Chronic Kidney Disease HP, diabetic nephropathy MESHD nephropathy HP

    Molecular Basis of Kidney Defects in COVID-19 Patients

    Authors: Smartya Pulai; Madhurima Basu; Chinmay Saha; Nitai P. Bhattacharyya; Arpita Ray Chaudhury; Sujoy Ghosh

    id:10.20944/preprints202007.0452.v1 Date: 2020-07-20 Source: Preprints.org

    Background: Kidney damage MESHD is considered to be one of the risk factors for severity and mortality among COVID-19 patients. However, molecular nature of such observations remains unknown. Hypothesis: Altered gene expressions due to infection and in chronic HP infection and in chronic MESHD chronic kidney disease MESHD could explain severity in COVID-19 with kidney defects MESHD. Methods: We collected gene expression data from publicly available resources Gene Expression Omnibus CKD MESHD, Enrichr for deregulated genes in SARS-CoV infected MESHD cells in vitro, DisGeNET and others and carried out enrichment analysis using Enrichr. Result: Number of common genes altered in chronic kidney disease HP chronic kidney disease MESHD ( CKD MESHD) and SARS-CoV infected MESHD cells was 2834. Enrichment analysis revealed that biological processes related viral life cycle and growth, cytokines, immunity, interferon, inflammation MESHD, apoptosis, autophagy, oxidative stress and others were significantly enriched with common deregulated genes. Similarly, significantly enriched pathways related to viral and bacterial infections MESHD, immunity and inflammation MESHD, cell cycle, ubiquitin mediated proteolysis, signaling pathways like Relaxin signaling pathway, mTOR signaling pathway, IL-17 signaling pathway, NF-kappa B signaling pathway were enriched with the common deregulated genes. These processes and pathways are known to be related to kidney damage MESHD. DisGeNET terms enriched include and related to Dengue fever MESHD fever HP, chronic Hepatitis HP chronic Hepatitis MESHD, measles, retroviridae infections MESHD, respiratory syncytial virus Infections MESHD and many others. Kidney dysfunction MESHD related terms ischemia of kidney, renal fibrosis MESHD renal fibrosis HP and diabetic nephropathy MESHD nephropathy HP. Conclusion: Common deregulated genes in SARS-CoV infected MESHD cells and chronic kidney disease HP chronic kidney disease MESHD, as well as their enrichment with molecular processes and pathways relevant for viral pathogenesis and renal dysfunctions MESHD, could explain the severity of COVID-19 with kidney disease MESHD. This observation not only provides molecular relation of severity in COVID-19 with renal dysfunctions MESHD but might also help in the management and treatment targets for these cases.

    SARS-CoV-2 receptor networks in diabetic kidney disease MESHD, BK-Virus nephropathy MESHD nephropathy HP and COVID-19 associated acute kidney injury HP kidney injury MESHD

    Authors: Rajasree Menon; Edgar A Otto; Rachel Sealfon; Viji Nair; Aaron K Wong; Chandra L Theesfeld; Xi Chen; Yuan Wang; Avinash Boppanna; Peter M Kasson; Jennifer A Schaub; Celine C Berthier; Sean Eddy; Chrysta C Lienczewski; Bradley Godfrey; Susan L Dagenais; Ryann Sohaney; John Hartman; Damian Fermin; Lalita Subramanian; Helen C Looker; Laura H Mariani; Abhijit S Naik; Robert G Nelson; Olga G. Troyanskaya; Matthias Kretzler

    doi:10.1101/2020.05.09.20096511 Date: 2020-05-13 Source: medRxiv

    COVID-19 morbidity and mortality is significantly increased in patients with diabetes MESHD and kidney disease MESHD via unknown mechanisms. SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) for entry into human host cells, and ACE2 levels in target cells may influence SARS-CoV-2 susceptibility. We investigated how pre-existing conditions and drug treatments alter receptor expression in kidney tissue. Using single cell RNA profiling (scRNAseq) to assess ACE2 and associated SARS-CoV-2 proteases in healthy living donors (LD) kidneys, diabetic kidney disease MESHD ( DKD MESHD), and in kidney injury MESHD during viral infection MESHD, ACE2 expression was primarily associated with proximal tubular epithelial cells (PTEC). ACE2 mRNA expression levels were significantly upregulated in DKD MESHD versus LD, however, ACE2 levels were not altered by exposures to renin angiotensin aldosterone system (RAAS) inhibitors. ACE2+ expression signatures were defined by differential expression analysis and characterized by Bayesian integrative analysis of a large compendium of public -omics datasets, resulting in the identification of network modules induced in ACE2 positive PTEC in DKD MESHD and BK virus nephropathy HP nephropathy MESHD. These ACE2 upregulated cell programs were linked to viral entry, immune activation, endomembrane reorganization, and RNA processing and overlapped significantly with the cellular responses induced by SARS-CoV-2 infection MESHD. Similar cellular programs were activated in ACE2-positive PTEC isolated in a urine sample from a COVID19 patient with acute kidney injury HP acute kidney injury MESHD, suggesting a consistent ACE2-coregulated expression program that may interact with SARS-Cov-2 infection MESHD processes. The SARS-CoV-2 receptor associated gene signatures could seed further research into therapeutic strategies for COVID-19. Functional networks of gene expression signatures are available for further exploration to researchers at HumanBase (hb.flatironinstitute.org/covid-kidney).

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MeSH Disease
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